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慢性心力衰竭时由于心输出量下降,机体的交感神经及肾素-血管紧张素-醛固酮系统(RAA 系统)被激活,以维持足够循环血压,但也引起血管收缩及体液潴留等神经内分泌紊乱。使用血管扩张剂治疗可使心输出量增加及心室充盈压下降,但长期用药后常出现失效或“耐受”现象,其原因可能与血管扩张剂加重心衰时存在的神经内分泌紊乱有关。为探讨RAA 系统在慢性心衰时的临床意义,作者对19例慢性心衰病人作双盲随机研究,给予血管紧张素转换酶抑制剂巯甲丙脯酸和交感神经系统α_1肾上腺素能受体阻滞荆哌唑嗪(prazosin)短期及长期治疗,对神经内分泌变化与临床及血液动力学反应之间的关系进行研究,其中16例完成了全部试验。
Chronic heart failure due to decreased cardiac output, the body’s sympathetic and renin - angiotensin - aldosterone system (RAA system) is activated to maintain adequate circulating blood pressure, but also cause vasoconstriction and fluid retention and other neuroendocrine disorders. The use of vasodilator therapy can increase cardiac output and ventricular filling pressure decreased, but often after long-term failure or “tolerance” phenomenon, the reason may be related to vasodilators exacerbating the presence of neuroendocrine disturbance of heart failure disorders. In order to investigate the clinical significance of RAA system in chronic heart failure, the authors conducted a double-blind randomized study on 19 chronic heart failure patients, giving angiotensin converting enzyme inhibitors captopril and sympathetic alpha 1 adrenergic receptor Blockade of short and long-term treatment with prazosin and study of the relationship between neuroendocrine changes and clinical and hemodynamic responses, 16 of which completed all trials.